Document Detail


Loss of fibulin-2 protects against progressive ventricular dysfunction after myocardial infarction.
MedLine Citation:
PMID:  22100229     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Remodeling of the cardiac extracellular matrix (ECM) is an integral part of wound healing and ventricular adaptation after myocardial infarction (MI), but the underlying mechanisms remain incompletely understood. Fibulin-2 is an ECM protein upregulated during cardiac development and skin wound healing, yet mice lacking fibulin-2 do not display any identifiable phenotypic abnormalities. To investigate the effects of fibulin-2 deficiency on ECM remodeling after MI, we induced experimental MI by permanent coronary artery ligation in both fibulin-2 null and wild-type mice. Fibulin-2 expression was up-regulated at the infarct border zone of the wild-type mice. Acute myocardial tissue responses after MI, including inflammatory cell infiltration and ECM protein synthesis and deposition in the infarct border zone, were markedly attenuated in the fibulin-2 null mice. However, the fibulin-2 null mice had significantly better survival rate after MI compared to the wild-type mice as a result of less frequent cardiac rupture and preserved left ventricular function. Up-regulation of TGF-β signaling and ECM remodeling after MI were attenuated in both ischemic and non-ischemic myocardium of the fibulin-2 null mice compared to the wild type counterparts. Increase in TGF-β signaling in response to angiotensin II was also lessened in cardiac fibroblasts isolated from the fibulin-2 null mice. The studies provide the first evidence that absence of fibulin-2 results in decreased up-regulation of TGF-β signaling after MI and protects against ventricular dysfunction, suggesting that fibulin-2 may be a potential therapeutic target for attenuating the progression of ventricular remodeling.
Authors:
Takeshi Tsuda; Jing Wu; Erhe Gao; Jennifer Joyce; Dessislava Markova; Hailong Dong; Ying Liu; Hangxiang Zhang; Yaqun Zou; Feng Gao; Thomas Miller; Walter Koch; Xingliang Ma; Mon-Li Chu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-11-09
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  52     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-26     Completed Date:  2012-04-24     Revised Date:  2014-08-11    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  273-82     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology
Animals
Calcium-Binding Proteins / deficiency*,  genetics
Extracellular Matrix Proteins / deficiency*,  genetics,  metabolism
Gene Expression
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Infarction / genetics*,  metabolism,  mortality
Myocardium / metabolism
Signal Transduction / drug effects
Transforming Growth Factor beta / metabolism
Ventricular Function, Left
Ventricular Remodeling / genetics*
Wound Healing / genetics
Grant Support
ID/Acronym/Agency:
GM55625/GM/NIGMS NIH HHS; P20 RR020173/RR/NCRR NIH HHS; P20 RR020173/RR/NCRR NIH HHS; R01 GM055625/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/Extracellular Matrix Proteins; 0/Transforming Growth Factor beta; 0/fibulin 2; 11128-99-7/Angiotensin II
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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